Transient Erythroblastopenia of Childhood
- Author: Lennox H Huang, MD; Chief Editor: Max J Coppes, MD, PhD, MBA more...
Background
Transient erythroblastopenia of childhood (TEC) is a slowly developing anemia that occurs in early childhood and is characterized by a gradual onset of pallor. As the name suggests, all patients with transient erythroblastopenia of childhood recover completely without sequelae.
Pathophysiology
The etiology of transient erythroblastopenia of childhood is unknown. However, researchers have proposed numerous viral and immunologic mechanisms. At least 2 separate case reports have noted pure red cell aplasia with concomitant human parvovirus B19 infection.[1, 2] However, a prospective case series of 10 patients failed to identify a single viral causative agent for transient erythroblastopenia of childhood.[3]
In vitro studies using serum and immunoglobulin G (IgG) from some patients with transient erythroblastopenia of childhood demonstrated erythroid colony suppression, suggesting an immunologic etiology. Transient erythroblastopenia of childhood is not caused by a lack of erythropoietin. Bone marrow from patients with transient erythroblastopenia of childhood exhibits an absence of red cell precursors.
A recent case report of half siblings with transient erythroblastopenia of childhood and the accompanying literature review suggests that predisposition to transient erythroblastopenia of childhood may be autosomal dominant in nature.[4]
Epidemiology
Frequency
United States
Attempts to determine frequency of transient erythroblastopenia of childhood are limited by an unknown number of asymptomatic undiagnosed cases.
Mortality/Morbidity
Morbidity relates to the severity of the anemia and diagnostic workup. Children with transient erythroblastopenia of childhood have reportedly presented with high-output shock secondary to profound anemia.[5] Patients with atypical transient erythroblastopenia of childhood may require invasive tests such as bone marrow aspiration or biopsy. Association of transient neurologic deficits may lead the physician to pursue CNS imaging studies or a neurologic consultation.
Sex
The male-to-female ratio is 1.4:1.
Age
The median age of presentation is 18-26 months; however, the disorder may occur in infants younger than 6 months and in children as old as 10 years. In contrast, Diamond-Blackfan anemia tends to present in child younger than 1 year, whereas human parvovirus B19–associated erythroblastopenia typically presents at an older age.
Prassouli A, Papadakis V, Tsakris A, et al. Classic transient erythroblastopenia of childhood with human parvovirus B19 genome detection in the blood and bone marrow. J Pediatr Hematol Oncol. Jun 2005;27(6):333-6. [Medline].
Geetha D, Zachary JB, Baldado HM, et al. Pure red cell aplasia caused by Parvovirus B19 infection in solid organ transplant recipients: a case report and review of literature. Clin Transplant. Dec 2000;14(6):586-91. [Medline].
Skeppner G, Kreuger A, Elinder G. Transient erythroblastopenia of childhood: prospective study of 10patients with special reference to viral infections. J Pediatr Hematol Oncol. May 2002;24(4):294-8. [Medline].
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Gustavsson P, Klar J, Matsson H, et al. Familial transient erythroblastopenia of childhood is associated with thechromosome 19q13.2 region but not caused by mutations in coding sequencesof the ribosomal protein S19 (RPS19) gene. Br J Haematol. Oct 2002;119(1):261-4. [Medline].
Krijanovski OI, Sieff CA. Diamond-Blackfan anemia. Hematol Oncol Clin North Am. Dec 1997;11(6):1061-77. [Medline].
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Mupanomunda OK, Alter BP. Transient erythroblastopenia of childhood (TEC) presenting as leukoerythroblastic anemia. J Pediatr Hematol Oncol. Mar-Apr 1997;19(2):165-7. [Medline].
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